title: Effects of renal perfusion pressure on renal interstitial hydrostatic pressure and Na+ excretion: role of endothelium-derived nitric oxide.
abstract: The purpose of this study was to examine the role of endothelium-derived nitric oxide in modulating the effect of renal perfusion pressure (RPP) on renal interstitial hydrostatic pressure (RIHP) and urinary Na+ excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and Na+ and Li+ excretions were determined in control Sprague-Dawley rats, in Sprague-Dawley rats pretreated with intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME) at doses of 1, 5, and 50 microg/kg/min, and in rats pretreated with L-NAME (5 microg/kg/min) plus L-arginine (10 mg/kg/min). The RPP was changed from 95 to 135 mm Hg by an electronically servo-controlled aortic occluder above the renal arteries in all groups. Increasing RPP in control rats from 95 to 135 mm Hg increased RIHP (from 4.4 +/- 0.5 to 8.7 +/- 1.2 mm Hg), UNaV (from 2.37 +/- 0.61 to 8.29 +/- 1.59 microEq/min), and fractional excretion of Li+ (from 38.0 +/- 2.5 to 51.4 +/- 6.0%). In rats pretreated with L-NAME (5 microg/kg/min), increases in RPP from 95 to 135 mm Hg had no effect on RIHP (from 1.6 +/- 0.4 to 2.2 +/- 0.6 mm Hg) or fractional excretion of Li+ and markedly attenuated pressure-natriuresis relationship (from 1.84 +/- 0.50 to 2.88 +/- 0.65 microEq/min). Although L-NAME did reduce renal plasma flow and glomerular filtration rate, the autoregulatory responses to RPP were maintained. In rats pretreated with L-NAME plus L-arginine, RIHP, UNaV, and fractional excretion of Li+ responses to RPP were similar to the control rats. The results of this study indicate that endothelium-derived nitric oxide plays an important role in modulating the effect of RPP on Na+ excretion by enhancing the transmission of RPP into the renal interstitium.
authors.affiliation: 2nd Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan. nakamurt@news.sb.gunma-u.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: A M
authors.initials: AM
authors.lastname: Alberola
authors.forename: F J
authors.initials: FJ
authors.lastname: Salazar
authors.forename: Y
authors.initials: Y
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Kurashina
authors.forename: J P
authors.initials: JP
authors.lastname: Granger
authors.forename: R
authors.initials: R
authors.lastname: Nagai
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D001835:Body Weight / Q000187:drug effects; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006874:Hydrostatic Pressure; D007668:Kidney / Q000502:physiology*; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000378:metabolism; D008094:Lithium / Q000652:urine; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000652:urine*
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D008094:Lithium; D012964:Sodium; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester